ArticlePloS one2016
miR-130b-3p Modulates Epithelial-Mesenchymal Crosstalk in Lung Fibrosis by Targeting IGF-1.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- A systematic review of overlapping microRNA patterns in systemic sclerosis and idiopathic pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2017Pooled it
- Development of a prognostic prediction signature for idiopathic pulmonary fibrosis by integrating multiple programmed cell death-related genes and machine learning algorithms.Journal of thoracic disease · 2025Article
- A Pilot Investigation of Circulating miRNA Expression in Individuals Exposed to Aluminum and Welding Fumes.Current issues in molecular biology · 2025Article
- Mechanisms of Bleomycin-induced Lung Fibrosis: A Review of Therapeutic Targets and Approaches.Cell biochemistry and biophysics · 2024Review
- Integrated bioinformatics analysis for the identification of idiopathic pulmonary fibrosis-related genes and potential therapeutic drugs.BMC pulmonary medicine · 2023Article
- Recent Advances (2015-2020) in Drug Discovery for Attenuation of Pulmonary Fibrosis and COPD.Molecules (Basel, Switzerland) · 2023Review
- Regulatory roles of noncoding RNAs in intervertebral disc degeneration as potential therapeutic targets (Review).Experimental and therapeutic medicine · 2023Review
- Role of MicroRNAs in Signaling Pathways Associated with the Pathogenesis of Idiopathic Pulmonary Fibrosis: A Focus on Epithelial-Mesenchymal Transition.International journal of molecular sciences · 2022Review
- Review
- Comparative computational RNA analysis of cardiac-derived progenitor cells and their extracellular vesicles.Genomics · 2022Article
- Evaluation serum levels of Insulin Growth Factor-1 (IGF-1) and its association with clinical parameters in severe COVID-19.Inflammopharmacology · 2022Article
- Expression of Concern: miR-130b-3p Modulates Epithelial-Mesenchymal Crosstalk in Lung Fibrosis by Targeting IGF-1.PloS one · 2022Article
- Article
- Long non‑coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA‑455‑3p/SMAD3 axis.Molecular medicine reports · 2021Article
- The function of non-coding RNAs in idiopathic pulmonary fibrosis.Open medicine (Warsaw, Poland) · 2021Review
- The Interplay Between Non-coding RNAs and Insulin-Like Growth Factor Signaling in the Pathogenesis of Neoplasia.Frontiers in cell and developmental biology · 2021Review
- Role of Non-Coding RNAs in Post-Transcriptional Regulation of Lung Diseases.Frontiers in genetics · 2021Review
- Approaches Toward Targeting Matrix Metalloproteases for Prognosis and Therapies in Gynecological Cancer: MicroRNAs as a Molecular Driver.Frontiers in oncology · 2021Review
- Long-distance chromatin interaction of IGF1 during embryonic and postnatal development in the liver of Sus scrofa.Functional & integrative genomics · 2021Article
- A novel prognostic model based on four circulating miRNA in diffuse large B-cell lymphoma: implications for the roles of MDSC and Th17 cells in lymphoma progression.Molecular oncology · 2021Article
Corrections and comments
- Expression of concern
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and usually lethal fibrotic lung disease with largely unknown etiology and pathogenesis. Evidence suggests microRNAs (miRNA) contribute to pathogenesis of IPF. In this study, we sought to identify miRNA expression signatures and determine the role of miR-130b-3p in lung fibrosis. The miRNA expression profile of the lungs from patients with IPF and normal donors was determined by Affymetrix microarray, and transcriptome with Affymetrix array. The functions and signal pathways as well as miRNA-mRNA networks were established by bioinformatics analysis. Luciferase assays and ELISA were used to confirm the miRNA target gene. The effect of miRNA-transfected epithelium on fibroblast activities was assessed using a co-culture system. The fibroblast activities were determined by qRT-PCR, western blotting, Transwell and BrdU assays. Seven miRNAs were significantly decreased in IPF lungs, with miR-130b-3p being the highest in the miRNA-mRNA network. Insulin-like growth factor (IGF-1) was a target gene of miR-130b-3p in the epithelium. miR-130b-3p inhibition in the epithelium induced collagen I expression and enhanced the proliferation and migration ability of fibroblast in co-culture systems, which mimicked the functions of exogenous IGF-1 on fibroblasts. Neutralizing IGF-1 with an antibody significantly reduced the modulatory effects of miR-130b-3p inhibitor-transfected epithelium on the activation of fibroblasts. Our results show that miR-130b-3p was downregulated in IPF lungs. miR-130b-3p downregulation contributed to the activation of fibroblasts and the dysregulated epithelial-mesenchymal crosstalk by promoting IGF-1 secretion from lung epithelium, suggesting a key regulatory role for this miRNA in preventing lung fibrosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.